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HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



L\'ED pressure also rises. As might be expected, the 

 divergence between a control VFC and one obtained 

 during restricted coronary blood flow is larger at the 

 higher filling pressures and stroke works; with 

 severer degrees of coronary blood flow restriction 

 not only will the plateau of the curve be lower but a 

 descending limb characteristic of the failing heart 

 will appear (23). With such techniques it has also 

 been possible to demonstrate acutely induced vini- 

 lateral ventricular failure (23). 



The observation that anemia also shifts V'FCla to 

 the right, in spite of the then obtaining higher coro- 

 nary blood flow, is evidence that, during coronary 

 flow restriction, a major influence producing the de- 

 pressed function is the limited oxygen availability 

 rather than the accumulation ot metabolites (24). 



B. The Atrium 



HETEROMETRic AUTOREGULATION. The Studies of 

 Blinks, who used a more highly refined technique for 

 studying atrial contractility than had previously 

 been available, ha\e dissoK'ed any possible reserva- 

 tions as to whether the force of atrial contraction is a 

 function of its end diastolic pressvire and volume 

 (fiber length) just as is the case with the \entricle 

 (10). He further demonstrated a shift of the atrial 

 function curve to the left under the influence of 

 catecholamines and also showed that, while imder 

 this influence, a change in atrial distensibility did 

 not take place (loa). Further evidence for hetero- 

 metric autoregulation in the atrium is seen in figure 

 1 1.4 (beats 1-19), a tracing obtained during the rapid 

 infusion of blood. As the infusion progressed and the 

 atrial pressures became elevated, atrial SNstole pro- 

 duced a progressively larger increment in both the 

 ventricular end diastolic pressure and segment length 

 indicating an augmented force of atrial contraction. 

 Evidence on which to base a judgment as to the 

 presence or absence of homeometric autoregulation 

 in the atrium is not presently a\ailable. 



EFFECT OF ATRIAL SYSTOLE ON LVED PRESSURE AND 



FIBER LENGTH. The significance of atrial systole for 

 ventricular filling was first shown by Harvey (46) 

 and later by Gesell (42), and Wiggers & Katz (126). 

 Harvey stated, ''At this same time when the auricles 

 alone are beating, if you cut off the lip of the heart 

 with a scissors, you will see blood gush out at each 

 beat of the auricles. This shows how blood enters the 

 ventricles, not by the suction or dilatation of tlie \'en- 

 triclcs, but l)\- the beat of the auricles." 



Recently it has become possible not only to make a 

 more definitive analysis of the influence of atrial 

 systole but also to designate those circumstances 

 under which atrial systole will produce more or less 

 diastolic lengthening of the ventricular myocardium 

 (58). The extent to which atrial systole can contribute 

 to the lengthening of the v^entricular myocardial fibers 

 can be seen in figure 10. In this record, obtained from 

 a dog with surgically induced heart block, there are 

 four atrial contractions for each ventricular contrac- 

 tion; the results of each atrial contraction can be 

 readily observed in the absence of disturbances 

 produced by ventricular actixity. Each atrial con- 

 traction, which produced only a small pressure rise in 

 the ventricle, caused a substantial increase in myo- 

 cardial segment length. The observed increases in 

 segment length thus induced were an appreciable 

 proportion of the total segment shortening which 

 took place during systole. 



The extent to which the level of \entricular diastolic 

 pressure will modify myocardial elongation due to 

 atrial systole is shown in figure i i. Figure i i.-l shows 

 41 consecutive beats during a rapidly administered 

 infusion. Figure i iB shows two beats at the beginning 

 and two beats at the end of a rapid infusion of blood. 

 In both, at the beginning of the infusion, when ven- 

 tricular diastolic pressure is low, the small increment 

 in end diastolic pressure consequent to atrial systole 

 is accompanied by a substantial segment length 

 elongation. At the end of the infusion, when the ven- 

 tricular diastolic pressure is high, atrial systole 

 causes a greater rise in pressure but a much dimin- 

 ished increase in segment length. This relationship 

 is expressed in the pressure-length curve of the ven- 

 tricle (fig. 12) which shows the plot of ventricular 

 diastolic pressure and changes in myocardial seg- 

 ment length during diastasis (58). Two successive 

 runs (circles and squares) were obtained by the 

 stepwise infusion of blood. When the diastolic pressure 

 in the ventricle is low, a small increment in pressure 

 produces a relatively large increase in myocardial 

 segment length (sensitive part). Conversely, at the 

 higher ventricular diastolic pressures only small in- 

 creases in segment length are produced by a similar 

 or even greater pressure increment (insensitive part). 



In the study of Lind and his colleagues (57), who 

 used contrast media for demonstrating the atrial 

 contribution to \eniricular filling in human heart 

 block, it was suggested that the atrial beats which 

 occurred early in diastole made a substantial con- 

 tribution to ventricular filling, whereas those which 

 occurred late in diastole contributed little to ventric- 



